Eyelid retractor surgery as an adjunct to cicatricial ectropion repair

Purpose : To evaluate the effectiveness of eyelid retractor repair in cicatricial ectropion of the lower eyelid. Methods : The study design was a prospective case series. One hundred and twenty eight eyelids were operated on in 100 consecutive patients with cicatricial ectropion. All patients underwent lower eyelid retractor repair via a conjunctival approach combined with skin replacement to the anterior lamella with or without a horizontal lid tightening procedure. When only medial ectropion was present, a medial‐based transpositional skin flap was used to repair the anterior lamella (26 eyelids). The remaining eyelids with ectropion involving all or most of the eyelid underwent upper‐to‐lower eyelid lateral‐based transpositional skin flap repair (92 eyelids), or full thickness free skin grafting (10 eyelids). Horizontal lid tightening was performed by lateral canthoplasty in 123 eyelids. Results : Relief of cicatricial ectropion symptoms was reported in 90% of patients overall. A normal punctum position was achieved in 70% of eyelids, overall, and was highest (88%) with a medial‐based transpositional skin flap. Conclusions : Eyelid retractor repair combined with skin replacement and horizontal lid shortening is an effective procedure for cicatricial ectropion.     

甲氨蝶呤治疗眼瘢痕性类天疱疮的疗效

目的：探讨应用甲氨蝶呤（MTX）治疗眼瘢痕性类天疱疮（OCP）的效果及安全性。方法：回顾性系列病例研究。收集2016年9月至2019年8月于天津医科大学总医院眼科行MTX治疗的OCP患者5例（10眼）,其中男2例,女3例。观察MTX治疗6个月、12个月OCP炎症的进展及药物不良反应。结果：本组患者OCP平均发病年龄51.8岁（38～66岁）,开始免疫治疗年龄54.4岁（39～68岁）。MTX治疗6个月,OCP好转3例,OCP部分活跃1例,OCP活跃1例。MTX治疗12个月,OCP好转4例,OCP活跃1例。活跃患者OCP睑球粘连进展,在MTX治疗12个月后加用利妥昔单抗联合治疗。治疗过程中,1人（1眼）在MTX治疗10个月时发生角膜病毒感染。另有2例应用MTX后出现轻度胃肠道反应,1例转氨酶轻度升高。随访期间无其他严重不良反应出现。结论：对于OCP患者,MTX耐受良好,早期应用有助于控制眼部病情。     

毛发移植治疗瘢痕性秃发的研究进展

瘢痕性秃发是一组毛囊被结缔组织取代的疾病,分为原发性和继发性。原发性瘢痕性秃发病情隐匿反复,早期以控制原发病为主,晚期病情稳定可考虑外科修复,术后需长期随诊、药物维持治疗。继发性瘢痕性秃发多继发于烧伤、手术,瘢痕稳定后可考虑手术治疗。本文就毛发移植治疗瘢痕性秃发的研究进展进行综述。     

Immunosuppressive Therapy for External Ocular Inflammatory Disease

Fourteen patients with progressive ocular inflammation and destructive lesions, unresponsive to conventional therapy, were treated with systemic immunosuppression. Ten patients had connective tissuelvasculitis diseases; two, cicatricial pemphigoid; and two, bilateral Mooren's corneal ulcers. Control of underlying systemic disease by immunosuppression resulted invariably in concomitant control of ocular inflammation and destruction. Encouraging results were obtained in the patients with cicatricial pemphigoid and those with bilateral Mooren's ulcers.     

Drug induced cicatrizing conjunctivitis: A case series with review of etiopathogenesis,diagnosis and management

Drug induced cicatrizing conjunctivitis (DICC) is defined as a disease in which conjunctival cicatrization develops as a response to the chronic use of inciting topical and, rarely, systemic medications. DICC accounts for up to one third of cases of pseudopemphigoid, a large group of cicatrizing conjunctival diseases sharing similar clinical features to those of mucous membrane pemphigoid (MMP) but generally without the morbidity of progressive scarring or the need for systemic immunosuppression. The preservatives in topical anti-glaucoma medications (AGM) are the most frequently implicated inciting causes of DICC although topical antivirals, vasoconstrictors and mydriatics and some systemic drugs have been implicated. The literature review summarizes the classification, epidemiology, etiopathogenesis, histopathology, clinical presentation, diagnosis, management, and treatment outcomes of DICC in the context of a case series of 23 patients (42 eyes) with AGM induced DICC, from India and the UK. In this series all subjects reacted to preserved AGM with one exception, who also reacted to non-preserved AGM. At diagnosis >70% of eyes showed punctal scarring, inflammation, and forniceal shortening. Pemphigoid studies were negative in the 19/23 patients in whom they were carried out. DICC can be classified as non-progressive, progressive with positive pemphigoid immunopathology or progressive with negative pemphigoid immunopathology. It is unclear whether progressive DICC is a stand-alone disease, or concurrent (or drug induced) ocular MMP. Progressive cases should currently be treated as ocular MMP. The diagnosis can be made clinically when there is rapid resolution of symptoms and inflammation, usually within 1–16 weeks, after withdrawal of suspected inciting medications, ideally by temporary substitution of oral carbonic anhydrase inhibitors. If the response to withdrawal is uncertain, or the progression of inflammation and scarring continues then patients must be evaluated to exclude concurrent (or drug induced) MMP, and other potential causes of CC, for which the treatment and prognosis is different. Management, in addition to withdrawing inciting medications, may require short-term treatment of conjunctival inflammation with steroids, treatment of associated corneal disease with contact lenses or surface reconstructive surgery, control of intra-ocular pressure with non-preserved AGM and, in some, surgery for glaucoma or for trichiasis and entropion.     

The 120-kDa soluble ectodomain of type XVII collagen is recognized by autoantibodies in patients with pemphigoid and linear IgA dermatosis

BACKGROUND: Type XVII collagen promotes adhesion of basal keratinocytes to epidermal basement membrane, and is the target of disease in patients with certain inherited or acquired blistering diseases. Two forms of type XVII collagen are produced by cultured human keratinocytes: a 180-kDa full-length, transmembrane protein, and a recently identified 120-kDa soluble fragment that corresponds to its collagenous ectodomain. OBJECTIVES: We aimed to determine the incidence and pattern of reactivity of autoantibodies against the 180- and 120-kDa forms of type XVII collagen in sera from 40 patients with bullous pemphigoid (BP), pemphigoid gestationis or cicatricial pemphigoid (CP), as well as six patients with linear IgA dermatosis (LAD). METHODS: Various immunochemical techniques were used. RESULTS: These studies found that the 120-kDa fragment of type XVII collagen was bound by circulating autoantibodies in 13 of 38 patients with BP or CP and all six patients with LAD. While many pemphigoid sera had specific reactivity against one but not both forms of this protein, autoantibodies from patients with LAD bound only the soluble ectodomain. CONCLUSIONS: These findings are consistent with the presence of both neoepitopes and cross-reactive epitopes on the ectodomain of type XVII collagen. The finding that sera from patients with LAD showed specific reactivity to epidermal basement membrane suggests that such neoepitopes are present in human skin and that their targeting by autoantibodies may contribute to disease pathogenesis.     

The use of intravenous immunoglobulin for treatment of dermatological conditions in Australia: A review

Intravenous immunoglobulin has been used in the treatment of various dermatological conditions, including toxic epidermal necrolysis, bullous pemphigoid and pemphigus vulgaris. From March 2008, the National Blood Authority has implemented the 'Criteria for the clinical use of intravenous immunoglobulins in Australia'. The new criteria have formalized the eligibility requirements for several dermatological conditions. This may increase access to intravenous immunoglobulin for treatment for these conditions. However, there remain stringent eligibility criteria with which dermatologists need to be acquainted. In some conditions, dermatology review is mandated by these criteria while in other conditions with skin manifestations, referral to other specialists is required. The following article provides a summary of the salient points in relation to the clinical use of intravenous immunoglobulin in dermatology, as well as its production and supply in Australia.     

Secondary cicatricial and other permanent alopecias

ABSTRACT:   Various nonfollicular scalp conditions can cause secondary scarring or permanent alopecia. Possible causes are congenital defects, trauma, inflammatory conditions, infections, and neoplasms (rarely drugs). Associated signs and symptoms and other diagnostic procedures such as histopathology may aid in the diagnosis. Detection of the underlying disorder may be difficult in end-stage lesions. Treatment is specific for active conditions. Surgery and hair transplantation are options for localized scars.     

Acquired scalp alopecia. Part I: A review

In this two-part series we review the acquired scalp alopecias. A broad spectrum of diseases result in alopecia. In this first part we provide a framework for the assessment and diagnosis of scalp hair loss, and begin covering the individual conditions. The non-scarring alopecias covered include effluvium, andro-genetic alopecia, alopecia areata, trichotillomania, and loose anagen syndrome. The scarring alopecias cause permanent pilosebaceous follicle loss; the lymphocyte-associated scarring alopecia described encompasses lichen planopilaris, discoid lupus erythematosus, pseudopelade, and follicular mucinosis. Part II will cover the neutrophil-associaled and infiltrative processes causing scarring alopecia followed by the medical management of alopecia. There is particular reference to newly described conditions and progress in the understanding of older conditions. More recently characterized conditions include the loose anagen syndrome, chronic telogen effluvium, and the frontal fibrosing variant of lichen planopilaris.